Glycitin Targets the Orphan Receptor GPR3 to Promote Milk Fat Synthesis in Goat Mammary Epithelial Cells

We examined glycitin-induced lipid synthesis in goat mammary epithelial cells (GMECs) and the involvement of G protein-coupled receptor 3 (GPR3). Glycitin increased triglyceride accumulation, lipid droplet formation, and lipogenic gene expression.

Docking and molecular dynamics suggested a plausible glycitin–GPR3 interaction, while the increase in cyclic adenosine monophosphate (cAMP) was weakened by <i>GPR3</i> knockdown. Glycitin also increased <i>GPR3</i> expression and reduced MYC-associated factor X (MAX)-associated transcriptional repression. <i>GPR3</i> knockdown reduced triglycerides, diacylglycerols, and fatty acid esters of hydroxy fatty acids (FAHFAs).